Association of Secondary Hyperparathyroidism with Red Cell Survival in Chronic Haemodialysis Patients

Saltissi, David; Carter, G. D.

doi:10.1042/cs0680029

Cited by 13 publications

(11 citation statements)

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“…The data of the present study and other results from our laboratory (10) as well as those of others (14) demonstrate that PTH satisfies most of the criteria for a uremic toxin (17) in regard to its action on the RBC in chronic renal failure. Its blood levels are elevated; it affects RBC in vitro by increasing their osmotic fragility; there is a direct relation between blood levels ofPTH and RBC survival in uremic patiepts; and RBC survival is normal in states of CRF without secondary hyperparathyroldism.…”

Section: Discussionsupporting

confidence: 64%

“…Saltissi and Carter (14) recently reported a significant inverse relationship (r = -0.67, P < 0.01) between RBC survival, as measured by 51Cr, and the blood levels ofPTH in 27 hemodialysis patients. They suggested that the secondary hyperparathyroidism of renal failure plays a major role in the genesis of the reduced RBC survival in these patients.…”

Section: Introductionmentioning

confidence: 99%

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Erythrocyte survival in chronic renal failure. Role of secondary hyperparathyroidism.

Akmal¹,

Telfer²,

Ansari³

et al. 1985

J. Clin. Invest.

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The human erythrocyte (RBC) is a target organ for parathyroid hormone (PTH) and the hormone increases RBC osmotic fragility and induces their hemolysis. The present study was undertaken to examine whether elevated blood levels of PTH affect RBC survival, and therefore whether PTH, being an extracorpuscular factor, is responsible for the shortened RBC survival in chronic renal failure. 51Cr-labeled RBC survival was elevated in six normal dogs, in six animals with chronic renal failure and secondary hyperparathyroidism (NPX), and in six thyroparathyroidectomized dogs (NPX-TPTX) with comparable degree and duration of chronic renal failure. In the normal dogs, 51Cr-labeled RBC survival ranged between 22 and 35 (25.6±1.9) d. In the NPX dogs, 51Cr-labeled RBC survival was shortened and the values ranged between 16 and 20 (18.4±0.6) d, a value significantly (P < 0.01) lower than normal dogs. In NPX-TPTX dogs, 5tCr-labeled RBC survival ranged between 20 and 33 (25.2±1.8) d, a value not different from that in normal dogs but significantly higher (P < 0.01) than that in NPX animals.Our data demonstrate that excess blood levels of PTH and not other consequences of the uremic state are responsible for the shortened RBC survival in chronic renal failure.

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Section: Discussionsupporting

confidence: 64%

Section: Introductionmentioning

confidence: 99%

Erythrocyte survival in chronic renal failure. Role of secondary hyperparathyroidism.

Akmal¹,

Telfer²,

Ansari³

et al. 1985

J. Clin. Invest.

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“…Lastly, we know very well the studies [8,9] cited by Massry and Akmal [1] : we agree that they provide impor tant findings in support of the theorized hemolytic effect of PTH in chronic renal failure. Yet, we found it difficult to quote such studies in our papers merely because they had not yet been published at that time.…”

mentioning

confidence: 55%

Osmotic Fragility of Erythrocytes and Secondary Hyperparathyroidism in Chronic Renal Failure

Docci¹

1987

Nephron

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The letter of Massry and Akmal, published in Nephron 43:70 (1986) [1], attacks harshly our previous papers [2,3] on the relation, if any, between red blood cell (RBC) osmotic fragility and secondary hyperparathyroidism (H PT) in chronic renal failure. We would like to have had a reply printed simultaneously; nevertheless, let us make some comments now.Firstly, Massry and Akmal [1] state that in the study of Bogin et al.[4] amounts of parathyroid hormone (PTH) only Vito 1 times higherthan normal were found to induce the maximum increase in the osmotic fragility of human RBC in vitro. Thus, since all our patients had exceedingly high blood levels of PTH, the lack of correlation between RBC osmotic fragility and serum PTH in these patients may be not unexpected. It is apparent that an important fact escaped these authors. We agree that the mean serum PTH concentration in our patients was 7-14 times more than normal, as stressed by Massry and Akmal [1]. Yet, as can be inferred by the wide standard deviation, a consid erable range in the individual values was observed. The patients studied indeed had serum PTH levels by be tween 1.4and 50.7 ng/ml (i.e., 0.56-56.6 times higherthan normal). It is in such patients that we failed to find a significant correlation between RBC osmotic fragility and serum PTH [2,3] [2,3], we found that the fall in the mean serum PTH concentration after treatment did not achieve statis tical significance because of the wide variation in the individual changes in the patients. Yet, according to Massry et al.[6], we think that such a treatment was all the same effective in controlling secondary HPT in our pa tients in view of the normalization or near normalization of serum alkaline phosphatase levels in them. Moreover, it should be remarked that in such patients the individual changes in RBC osmotic fragility in response to treat ment with l,25-(OH)2D3 did not correlate with the respec tive changes in serum PTH [2,3] and that no improvement in RBC osmotic fragility was observed in 2 patients after parathyroidectomy in the face of the substantial decrease in serum PTH in both [2].In our opinion, these findings speak strongly against at least the third and fourth criteria recommended by Massry himself [7] to consider a substance responsible for a given uremic manifestation. All things considered, our data can allow the conclusion that secondary HPT is probably not a 'major' factor influencing RBC osmotic fragility in chronic renal failure.Lastly, we know very well the studies [8,9] cited by Massry and Akmal [1] : we agree that they provide impor tant findings in support of the theorized hemolytic effect of PTH in chronic renal failure. Yet, we found it difficult to quote such studies in our papers merely because they had not yet been published at that time. Vice versa, had Massry and Akmal read the 'previous' literature care fully, our papers included, they would have been more prudent in the conclusions they drew [9], We think that the role of PTH as uremic toxin is still quite a debatable i...

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“…We used GOT as marker enzyme for the age determination of erythro cytes. The density distribution of RBCs dif fers only slightly between healthy subjects and hemodialysis patients whereas all RBC density fractions of hemodialysis patients show significantly higher GOT activity as an expression of reduced life span, which has been frequently demonstrated by 5lCr studies [5,10,14,15]. Erythrocytes of hemodialysis patients do not only exhibit elevated GOT activities but also elevated pyruvate kinase, hcxokinase and glucose 6-phosphate dehy drogenase activities [16].…”

Section: Discussionmentioning

confidence: 99%

“…2 ml filtered blood each were layered on the top of 12 ml of a continuous Percoll density gradient solu tion and centrifuged for 10 min at 10,000 g in a Sorvall centrifuge at 4 °C. The density gradient solution was obtained by centrifugation of a 50% Percoll solu tion in HEPES buffer for 10 min at 10,000# and 4 °C in a Sorvall centrifuge [10]. The separated erythro cytes were collected from the bottom of the vial in 500-pl fractions using a glass capillary.…”

Section: Methodsmentioning

confidence: 99%

Erythropoiesis and Erythrocyte Age Distribution in Hemodialysis Patients Undergoing Erythropoietin Therapy

Hampl¹,

Riedel²,

Scigalla³

et al. 1990

Blood Purif

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Renal anemia is caused in part by a reduced life span of red blood cells (RBCs) and by reduced erythropoietin biosynthesis in the damaged kidney. The RBC age can be determined by density gradient centrifugation and estimation of cell-age-dependent enzyme activities, as aspartate aminotransferase. The RBC age distribution influences the median density (D50) of RBCs and the blood rheology in coherence with the hematocrit. In our study, the median density was determined by Percoll density gradient centrifugation in 18 healthy subjects (D₅₀ = 1.0674 ± 0.0016 g/ml) and in 14 hemodialysis patients (D₅₀ = 1.0674 ± 0.0016 g/ml in the course of recombinant human erythropoietin (rhEPO) therapy. During the first 4 weeks of therapy, a strong rejuvenation of RBCs was observed whereby the D₅₀ reached a minimum after 2 weeks (D₅o = 1.0655 ± 0.0022 g/ml; p < 0.05 vs. value before therapy) and a steady state after 4 weeks (D₅₀ = 1.0658 ± 0.0013 g/ml; p < 0.1 vs. value before therapy). In 5 of the patients with elevated plasma parathyroid hormone (i-PTH) concentrations > 10pmol/l, a significantly (p < 0.05) reduced amount of younger RBCs (D₅₀ = 1.0675 ± 0.0016 g/ml) was observed in the first 2 weeks of rhEPO therapy as compared to patients with i-PTH < 10 pmol/l (D₅₀ = 1.0677 ± 0.0019 g/ml). Thus, erythropoiesis in the early phase of rhEPO therapy is strongly influenced by elevated plasma i-PTH concentrations. Therefore, a gradual increase in rhEPO doses is preferable before therapy at elevated doses with an uncontrolled increase in RBC amount.

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Association of Secondary Hyperparathyroidism with Red Cell Survival in Chronic Haemodialysis Patients

Cited by 13 publications

References 0 publications

Erythrocyte survival in chronic renal failure. Role of secondary hyperparathyroidism.

Erythrocyte survival in chronic renal failure. Role of secondary hyperparathyroidism.

Osmotic Fragility of Erythrocytes and Secondary Hyperparathyroidism in Chronic Renal Failure

Erythropoiesis and Erythrocyte Age Distribution in Hemodialysis Patients Undergoing Erythropoietin Therapy

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